The Association between Exposure to Second-Hand Smoke and Disease in the Chinese Population: A Systematic Review and Meta-Analysis

Objective To analyze the association between exposure to second-hand smoke(SHS) and 23 diseases,categorized into four classifications, among the Chinese population.Methods We searched the literature up to June 30, 2021, and eligible studies were identified according to the PECOS format: Participants and Competitors(Chinese population), Exposure(SHS),Outcomes(Disease or Death), and Study design(Case-control or Cohort).Results In total, 53 studies were selected. The odds ratio(OR) for all types of cancer was 1.79(1.56–2.05), and for individual cancers was 1.92(1.42–2.59) for lung cancer, 1.57(1.40–1.76) for breast cancer, 1.52(1.12–2.05) for bladder cancer, and 1.37(1.08–1.73) for liver cancer. The OR for circulatory system diseases was 1.92(1.29–2.85), with a value of 2.29(1.26–4.159) for stroke. The OR of respiratory system diseases was 1.76(1.13–2.74), with a value of 1.82(1.07–3.11) for childhood asthma. The original ORs were also shown for other diseases. Subgroup analyses were performed for lung and breast cancer. The ORs varied according to time period and were significant during exposure in the household;For lung cancer, the OR was significant in women.Conclusion The effect of SHS exposure in China was similar to that in Western countries, but its definition and characterization require further clarification. Studies on the association between SHS exposure and certain diseases with high incidence rates are insufficient.

Dynamic Expression of Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor in Rat Model of Pulmonary Emphysema Induced by Smoke Exposure

In order to explore the roles of tumor necrosis factor-α （TNF-α） and vascular endothelial growth factor （VEGF） in the pathogenesis of pulmonary emphysema, male Wistar rats were randomized into group At, group A2.5 and group A4, each with smoke exposure for 1 month, 2.5 months or 4 months, respectively. Group B t, group B2.5 and group B4 were used as non smoking controls at corresponding time points. TNF-α in bronchoalveolar lavage fluid （BALF） and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either. Lung slices were stained with hematoxylin and eosin （HE）. Results showed that in animal with smoke exposure the mean linear interceptor （Lm）, an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually, on contrary, the expression of VEGF in lung tissue decreased （P〈0.05）. This phenomenon was not obvious in animals without smoke exposure. Lm was negatively correlated to the VEGF expression （7=--0.81, P〈0.01） and positively correlated to TNF-α concentration （7 = 0.52, P〈0.004）, which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α. It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.

Association between Tobacco Smoke Exposure (Environmental and Direct) and Incidence and Control of Bronchial Asthma

Background: Asthma is a chronic multifactorial disease with high prevalence. Among asthma risk factors, the effect of tobacco smoke exposure on bronchial asthma is still debated. Aim: The aim of this study was to determine the association between environmental and direct tobacco smoke (cigarette and hookah) exposure and incidence and control of bronchial asthma. Materials & Methods: This descriptive study was conducted on 109 patients with asthma referring to Imam Khomeini Hospital in Ardabil city. Asthma Control Questionnaire was used for evaluating of asthma control. Patients’ asthma control was individually evaluated and compared with together with particular attention to history of tobacco smoke exposure. Chi square and Tav-Kendal were used to analyze the data in SPSS15 software. Results: The history of tobacco smoke exposure was found in 31.2% of the 109 patients. Patients with uncontrolled asthma with 60.6% constituted the largest volume of all samples. There was no significant correlation between tobacco smoke exposure and asthma occurrence (P > 0.05), also there was not found significant correlation between tobacco smoke exposure and asthma control (Error coefficient > 0.10). Conclusion: According to the results, history of tobacco (cigarette and hookah) smoke exposure (environmental and direct) has no effect on the asthma occurs and control status.

Impact of Smoke-Free Legislation on Acute Myocardial Infarction and Subtypes of Stroke Incidence in Shenzhen,China,2012-2016:An Interrupted Time Series Analysis

Objective This study assesses the impact of smoke-free legislation on the incidence rate for acute myocardial infarction(AMI)and stroke in Shenzhen.Methods Data on ischemic(n=72,945)and hemorrhagic(n=18,659)stroke and AMI(n=17,431)incidence covering about 12 million people in Shenzhen from 2012 to 2016 were used.Immediate and gradual changes in incidence rates were analyzed using segmented Poisson regression.Results Following the smoke-free legislation,a 9%(95%CI:3%-15%)immediate reduction was observed in AMI incidence,especially in men(8%,95%CI:1%-14%)and in those aged 65 years and older(17%,95%CI:9%-25%).The gradual annual benefits were observed only in hemorrhagic and ischemic stroke incidence,with a 7%(95%CI:2%-11%)and 6%(95%CI:4%-8%)decrease per year,respectively.This health effect extended gradually to the 50-64 age group.In addition,neither the immediate nor gradual decrease in stroke and AMI incidence rates did not show statistical significance among the 35-49 age group(P>0.05).Conclusion Smoke-free legislation was enforced well in Shenzhen,which would generate good experiences for other cities to enact and enforce smoke-free laws.This study also provided more evidence of the health benefits of smoke-free laws on stroke and AMI.

河北省初中生尝试吸烟行为及影响因素分析

目的了解河北省初中生尝试吸烟情况及相关影响因素,为开展控烟干预工作和提出控烟政策提供支持。方法2021年8—11月采用多阶段分层整群随机抽样方法,抽取河北省初中在校学生为调查对象,使用中国疾病预防控制中心制定的《2021年中国青少年烟草流行调查问卷》,调查学生基本情况、烟草使用情况、二手烟暴露和烟草广告获取等信息,分析学生尝试吸烟情况及其影响因素。结果河北省31486名初中生中,尝试吸烟者3049人,加权后尝试吸烟率为9.42%(95%CI:8.00~11.05),男生明显高于女生,差异有统计学意义(P<0.05);过去30 d内有过烟草广告及促销暴露的学生为17139人,烟草广告及促销暴露率为54.36%,其中,在电视或视频暴露最高比例为48.67%(95%CI:46.65%~50.70%),其次在互联网暴露比例为15.41%(95%CI:14.60%~16.27%);多因素Logistic回归分析结果显示,男生(OR=1.594,95%CI:1.997~2.709)、二年级(OR=1.320,95%CI:1.108~1.574)、1周零花钱>40元(OR=1.412,95%CI:1.253~1.592)、父母吸烟(OR=1.260,95%CI:1.078~1.472)、朋友吸烟(OR=6.680,95%CI:5.482~8.141)、教师吸烟(OR=1.686,95%CI:1.410~2.016)、二手烟暴露(OR=3.084,95%CI:2.667~3.566)、烟草广告及促销暴露(OR=1.451,95%CI:1.259~1.674)因素为初中生尝试吸烟的危险因素,接触过媒体控烟信息(OR=0.617,95%CI:0.555~0.685)是初中生尝试吸烟的保护因素。结论河北省初中生尝试吸烟率较高,烟草广告暴露情况较为严重,今后应净化社会、校园及周边环境烟草广告及促销对学生的影响,减少学生尝试吸烟行为的发生。

红景天苷调控NF-κB、Bcl-2信号通路对烟雾暴露大鼠氧化应激及肺血管内皮细胞凋亡的影响

目的探究红景天苷(SDS)通过调控B淋巴细胞瘤-2(Bcl-2)、核转录因子-κB(NF-κB)信号通路对烟雾暴露大鼠氧化应激及肺血管内皮细胞凋亡的机制。方法选取60只大鼠分为对照组、模型组、SDS 10 mg/kg、SDS 40 mg/kg、SDS 70 mg/kg、醋酸泼尼松(PNS)组,每组10只,除对照组外,其余均建立烟雾致肺损伤模型,对照组与模型组大鼠每日采用等量生理盐水灌胃;SDS高、中、低剂量组分别按70、40、10 mg/kg剂量给予SDS混悬液2 mL灌胃;PNS组给予PNS混悬液3.6 mg/kg灌胃,均每日1次,连续21 d。结果与对照组比较,模型组大鼠血清中丙二醛(MDA)、Bcl-2相关X因子(Bax)、NF-κB、p-NF-κB及细胞凋亡升高,超氧化物歧化酶(SOD)、Bcl-2降低(P<0.05);与模型组比较,SDS各剂量组MDA、Bax、NF-κB、p-NF-κB及细胞凋亡均有所降低,SOD、Bcl-2也有所升高(P<0.05),且模型组与SDS 10 mg/kg组比较无明显差异(P>0.05),SDS 40 mg/kg组与PNS组比较无明显差异(P>0.05)。对照组大鼠肺组织良好;模型组肺损伤严重;药物干预后各组肺损伤均减轻。结论SDS可改善烟雾暴露大鼠肺损伤、氧化应激及血管内皮细胞凋亡,其机制可能与调控Bax/Bcl-2及NF-κB相关。

二手烟暴露与孤独症谱系障碍患病风险关联的系统综述和Meta分析

目的基于观察性研究,采用Meta分析探索二手烟暴露与孤独症谱系障碍(autism spectrum disorder,ASD)风险的关联,以探究二手烟与ASD风险关联的关键暴露窗口。方法检索Ovid、EMBASE、Web of Science、Cochrane Library、PubMed、中国知网、万方数据库,检索时限为自建库起至2023年4月30日。纳入二手烟暴露与ASD风险的相关研究,进行质量评估,采用推荐、评估、发展和评价分级系统(The Grading of Recommendations,Assessment,Development,and Evaluation,GRADE)及最佳证据综合(The Best Evidence Synthesis,BES)方法进行证据强度评价,根据异质性应用随机效应模型或固定效应模型进行Meta分析。结果本研究纳入36篇观察性研究,Meta分析结果显示,孕期和1岁以后的二手烟暴露与ASD患病风险相关(孕期:OR=1.79,95%CI:1.20~2.68;1岁以后:OR=1.39,95%CI:1.10~1.75),但两种证据强度评价结果均显示强度较低。亚组分析未发现异质性来源,敏感性分析显示结果稳定,剪补法提示现问卷/报告/访谈形式收集二手烟暴露信息的所有暴露时期暴露组可能存在发表偏倚。结论孕期和1岁以后二手烟暴露会增加后代ASD患病风险,未发现其他时期与ASD相关。但受证据强度低的限制,未来应进一步采用高质量研究以验证此关联。

典型室内吸烟环境细颗粒物与黑碳动态变化及人群暴露特征

中国大多数城市尚未出台室内控烟法令,导致公共环境室内吸烟行为较为普遍,对室内空气质量和相关风险人群的健康造成了严重危害。目前仍缺乏研究表征吸烟引发的室内空气污染及其动态变化特征,阻碍了控烟政策的制定。本研究基于高时间分辨率在线细颗粒物(PM_(2.5))和黑碳(BC)监测仪,结合相关风险人群暴露特征调研数据,探究了典型吸烟环境(棋牌室)的室内污染水平、动态变化特征、影响因素和吸烟导致的污染物排放强度及风险人群的额外暴露。结果表明棋牌室日均PM_(2.5)和BC浓度分别为(154±68.9)mg·L^(-1)和(3.7±1.4)mg·L^(-1),其中营业期间的浓度为非营业期间浓度的6.5倍和2.6倍。PM_(2.5)和BC浓度的室内外比值(I/O)分别为6.3和4.1,表明室内源排放是棋牌室空气污染的主要来源。吸烟可以迅速升高室内PM_(2.5)和BC浓度并产生浓度峰,峰值可达(502±111)mg·L^(-1)和(8.5±2.9)mg·L^(-1)。吸烟导致棋牌室PM_(2.5)和BC的排放强度分别为(332±218)mg·L^(-1)·min^(-1)和(3.2±1.8)mg·L^(-1)·min^(-1),风险人群因吸烟导致的日均PM_(2.5)和BC的额外暴露分别为74.5 mg·L^(-1)和0.67 mg·L^(-1),年均额外暴露分别为21.3 mg·L^(-1)和0.19 mg·L^(-1),表明室内吸烟引发的额外暴露会导致严重的健康风险。本研究为吸烟导致的室内空气污染提供了基础数据,研究结果可为控烟政策制定提供科学支撑。

miRNA-138-5p靶向调控胱天蛋白酶3减缓吸烟所致睾丸支持细胞TM4细胞凋亡

近年来研究表明,长期大量吸烟可致睾丸出现不可逆性损伤进而出现精子发生受阻,凋亡信号通路在其中发挥着关键作用,其分子调控机制仍有待深入研究。本研究旨在探讨miRNA-138-5p在香烟烟雾所致小鼠睾丸支持细胞TM4细胞(正常小鼠睾丸Sertoli细胞)损伤中的靶向调控机制。MTT法、乳酸脱氢酶法和TUNEL法结果显示,CSE干预后的TM4细胞存活率显著降低(P<0.05),细胞毒性显著增加(P<0.05),细胞凋亡率显著增加(P<0.05);RT-PCR和Western印迹结果证明,10%CSE干预TM4细胞后,凋亡前体基因p53、促凋亡基因Bak和胱天蛋白酶3(caspase-3)的mRNA和蛋白质表达水平显著上调(P<0.05);在TM4细胞中转染miRNA-138-5p过表达质粒后同样进行CSE干预,结果显示,支持细胞存活率较转染前显著升高(P<0.05),凋亡阳性细胞数较转染前显著降低(P<0.05),凋亡前体p53基因、促凋亡基因Bak和Caspase-3的mRNA和蛋白质表达较转染前显著下调(P<0.05);沉默miRNA-138-5p后,Bak、胱天蛋白酶3的mRNA和蛋白质表达水平显著增加(P<0.05);在线数据库分析显示,miRNA-138-5p与胱天蛋白酶3具有较高的匹配预测值,双荧光素酶报告基因结果显示,Bak未结合至miRNA-138-5p,而胱天蛋白酶3可以靶向结合至miRNA-138-5p。以上结果提示,miRNA-138-5p可靶向调控胱天蛋白酶3,减缓吸烟所致睾丸支持细胞凋亡,具有支持细胞的保护作用。

家庭环境二手烟暴露对青少年情绪行为的影响

目的分析家庭环境二手烟暴露对青少年情绪行为的影响,为从家庭环境方面干预青少年情绪行为问题的发生发展提供理论支持。方法调查重庆市主城某区1002名青少年的家庭基本信息、家庭环境二手烟暴露、青少年自评量表(Youth Self-Report,YSR)等情况,使用多因素Logistic回归模型分析青少年家庭环境二手烟暴露与其情绪行为间的关系。结果48.2%的青少年存在家庭环境二手烟暴露问题。家庭环境二手烟暴露与未暴露的青少年整体情绪行为问题平均得分分别为(26.83±22.28)分和(23.61±20.33)分,整体情绪行为问题的检出率分别为12.2%和8.3%。多因素Logistic回归分析结果显示,存在整体情绪行为问题的青少年中,家庭环境二手烟暴露的青少年多于未暴露的,OR值为1.838(95%CI:1.161~2.911);女性青少年多于男性,OR值为2.476(95%CI:1.546~3.964);年龄较大的青少年多于年龄较小的,OR值为1.440(95%CI:1.186~1.749);父亲在外地工作的青少年多于父亲没有在外地工作的,OR值为2.511(95%CI:1.271~4.959);自觉父母间关系一般和较差的青少年多于自觉父母间关系较好的,OR值分别为2.791(95%CI:1.643~4.743)和3.879(95%CI:1.607~9.367);且家庭环境二手烟暴露的青少年内化行为问题多于未暴露的青少年,OR值为1.568(95%CI:1.015~2.422)。结论本研究中约50%的青少年存在家庭环境二手烟暴露问题,家庭环境二手烟暴露是影响青少年内化行为问题和整体情绪行为问题的重要因素。

慢性阻塞性肺疾病大鼠模型的建立与比较

目的通过单独烟草烟雾暴露(cigarette smoke exposure,CSE)或CSE联合脂多糖(lipopolysaccharide,LPS)、猪胰弹性蛋白酶(porcine pancreatic elastase,PPE)气管内滴注2种方法构建慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)大鼠模型并比较造模效果。方法SPF级雄性SD大鼠30只,随机分为对照组、烟熏组、联合组,每组10只,分别予正常环境饲养、CSE、CSE联合LPS及PPE气管内滴注。每周检测大鼠体重,4周后检测大鼠肺功能,HE染色观察肺组织病理变化,测定血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-8(interleukin-8,IL-8)及肺组织中黏蛋白5AC(mucin 5 subtype AC,MUC5AC)水平。结果烟熏组、联合组大鼠体重显著低于对照组(P<0.05);联合组大鼠体重明显低于烟熏组(P<0.05)。联合组用力肺活量(forced vital capacity,FVC)显著低于对照组(P<0.05),烟熏组、联合组大鼠第0.3 s用力呼气量(forced expiratory volume in 0.3 s,FEV0.3)、FEV0.3/FVC水平显著低于对照组(P<0.05);联合组大鼠FEV0.3、FVC、FEV0.3/FVC水平显著低于烟熏组(P<0.05)。烟熏组与联合组肺泡腔均呈扩大融合;联合组可见间隔变薄、断裂,融合成肺大泡。烟熏组、联合组大鼠血清TNF-α、IL-8及肺组织MUC5AC水平明显高于对照组(P<0.05);联合组大鼠血清TNF-α、IL-8及肺组织MUC5AC水平明显高于烟熏组(P<0.05)。结论以上2种方法均能成功构建COPD大鼠模型,CSE联合LPS、PPE气管内滴注建立的模型比单纯CSE建立的模型更符合COPD患者的临床特点及病理特点。

烟雾诱导慢性阻塞性肺疾病小鼠模型合并抑郁的评估

目的 探究单纯烟草烟雾慢性暴露诱导的慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)小鼠模型能否合并发生抑郁。方法 SPF级小鼠分为对照组(CTL组)和烟雾暴露组(CS组)。将CS组小鼠连续24周暴露在烟草烟雾中,最后一次烟熏24 h后进行旷场测试、悬尾测试,再进行肺功能检测。ELISA检测支气管肺泡灌洗液(BALF)上清中炎症因子白细胞介素-6(IL-6)、角质形成细胞衍生趋化因子(KC)的水平变化,以及血清中5-羟色胺(5-HT)的含量变化。H&E染色和尼氏染色观察小鼠肺组织、脑组织的病理学变化。结果 与CTL组相比,CS组小鼠体质量增长缓慢(P <0.001),肺功能检测FRC、FVC显著升高(P <0.001),FEV20/FVC和FEV50/FVC显著降低(P <0.05);CS组小鼠的BALF中IL-6、KC的表达水平升高(P <0.01),血清中5-HT水平明显降低(P <0.001);旷场实验中CS组小鼠的运动总路程、进入中央区次数、中央区滞留时间均降低(P <0.05),悬尾测试中CS组小鼠的静止不动时间增加(P <0.05);H&E染色显示CS组的肺组织平均肺泡截距显著增加(P <0.001),尼氏染色显示CS组小鼠皮质(P <0.001)和海马区(P <0.01)受损的神经元数量显著增加。结论 单纯烟草烟雾慢性暴露诱导的COPD小鼠模型可合并抑郁发生。

非吸烟相关性脱屑性间质性肺炎1例

脱屑性间质性肺炎是较为罕见的特发性间质性肺病,需要经病理明确,国内个案报道不多,而非吸烟脱屑性间质性肺炎更为少见,2019年7月10日上海市松江区中心医院行经皮肺穿活检发现1例,报道如下。

Repeated exposure to moxa-burning smoke: its acute and chronic toxicities in rats

OBJECTIVE: To assess toxicities of the air in Chi-nese medicine clinics polluted by moxa-burning smoke due to moxibustion-derived burning products(MBP).METHODS: Both acute and chronic toxicity studies were conducted. For the acute toxicity study, five groups of Wistar rats(n = 16/group, male: female =1∶1) were exposed to five different concentrations(95%, 90%, 85%, 80% and 75%, respectively) of MBP for 2 h. For the chronic toxicity study, another three groups of male rats(n = 21/group) were exposed to MBP in three concentrations(10%, 40%and 70%, respectively) and one control group exposed to clean air 20 min/d for 144 d. Routine examinations were performed and analyzed by analysis of variance and dose-response relationship.RESULTS: In the acute toxicity study, the number of dead rats in the 95%, 90%, 85%, 80% and 75%groups were 16, 13, 7, 6 and 3, respectively, with LD50 of 86.274% after or during the 2 h exposure.In the chronic toxicity study, MBP exposure induced a decline in activity of the rats. Rats in the10% group showed no signs of toxicity, while those in the 40% MBP group showed toxicity effects on the body weights(P < 0.05) and lung. Rats in the70% MBP group also presented with reversible damage in the blood coagulation system(P < 0.05).CONCLUSION: Exposure to 10% MBP, which is equivalent to 27.45 mg/m3, was under the critical threshold for male rats' safety. Exposure to MBP above that limit induced lung damage. MBP in clinics need to be reduced to a safe level with enhanced ventilation.

云南省成人烟草危害和二手烟暴露认知状况调查

目的了解云南省≥15岁居民烟草危害和二手烟暴露致病的认知现状,为有针对性地开展控烟健康教育提供支持。方法采用分层多阶段整群随机抽样法,抽取云南省12个州市24个项目点的6369人作为调查对象。使用全球烟草监测系统问卷进行入户调查。结果云南省≥15岁成人的吸烟率为32.2%(95%CI:30.4%~34.1%),戒烟率为13.6%(95%CI:11.7%~15.7%),二手烟暴露率为82.8%(95%CI:79.8%-85.5%)。电子烟的现在使用率为0.9%(95%CI:0.5%~1.7%)。吸烟导致肺癌、心脏病、中风和勃起障碍四种疾病的知晓率分别为80.0%(95%CI:75.2%~84.0%)、51.8%(95%CI:46.5%~57.1%)、39.6%(95%CI:34.2%~45.3%)和30.9%(95%CI:24.9%~37.6%);吸烟导致四种疾病的全知晓率为22.0%(95%CI:16.8%~28.3%)。二手烟暴露导致儿童肺部疾病、成人肺癌、成人心脏病三种疾病的知晓率分别为56.8%(95%CI:51.7%~61.8%)、51.5%(95%CI:47.1%~55.9%)和33.4%(95%CI:28.9%~38.2.3%);二手烟暴露导致三种疾病的全知晓率为28.9%(95%CI:24.8%~33.4%)。云南省成人对“低焦油不等于低危害”正确认知的比例仅为6.6%(95%CI:5.1%~8.5%)。多因素logistic回归分析显示,性别、居住地、年龄、文化程度及是否吸烟均是烟草烟雾致病全知晓率的影响因素。结论云南成人对吸烟和二手烟暴露导致的疾病知晓率较低且认识较片面,对二手烟危害的认知明显低于对吸烟危害的认知,缺乏对二手烟说不的态度。

Adult Secondhand Smoke Exposure—Shanghai Municipality,2018

Summary What is already known on this topic?The average secondhand smoke exposure rate was 68.1%in China in 2018.The World Health Organization suggests that legislation must be used to achieve a 100%smoke-free environment and protect nonsmokers from secondhand smoke.What is added by this report?

烟草烟雾暴露的人支气管上皮细胞铁死亡情况观察及其机制

目的观察烟草烟雾暴露对体外培养的人支气管上皮细胞铁死亡的影响并分析其机制。方法正常人支气管上皮细胞BEAS-2B分别使用0、0.5%、1.0%和2.0%的烟草烟雾提取物(CSE)处理24 h,即为对照组、0.5%CSE组、1.0%CSE组及2.0%CSE组。采用EdU染色观察细胞增殖能力,CCK-8法观察细胞活性;比色法检测细胞Fe2+水平和还原型谷胱甘肽(GSH)水平;流式细胞术观察细胞活性氧(ROS)水平;q-PCR法及Western blotting法观察铁死亡相关因子谷胱甘肽过氧化酶4(GPx4)、铁蛋白重链1(FTH1)及环加氧酶2(Ptgs2)mRNA及蛋白;碘化丙啶染色观察细胞死亡情况;透射电镜观察细胞线粒体结构。将BEAS-2B细胞分为Fer-1组、Nec-1组、Z-VAD-FMK组及CSE组,分别给予铁死亡抑制剂Fer-1、坏死抑制剂Nec-1、凋亡抑制剂Z-VAD-FMK及不加试剂预处理后,加入2.0%CSE培养基处理24 h。采用CCK-8法观察各组细胞活性;比色法检测Fer-1组、CSE组细胞Fe2+及GSH水平,流式细胞术观察Fer-1组、CSE组细胞ROS水平;q-PCR法及Western blotting法观察Fer-1组、CSE组细胞FTH1、Ptgs2、GPx4mRNA及蛋白表达;碘化丙啶染色观察Fer-1组、CSE组细胞死亡情况。结果EdU阳性细胞数、细胞OD值对照组>0.5%CSE组>1.0%CSE组>2.0%CSE组;细胞Fe2+水平、ROS水平对照组<0.5%CSE组<1.0%CSE组<2.0%CSE组,GSH水平对照组>0.5%CSE组>1.0%CSE组>2.0%CSE组;细胞FTH1、GPx4 mRNA及蛋白对照组>0.5%CSE组>1.0%CSE组>2.0%CSE组,Ptgs2 mRNA及蛋白对照组<0.5%CSE组<1.0%CSE组<2.0%CSE组;细胞死亡率对照组<0.5%CSE组<1.0%CSE组<2.0%CSE组(P均<0.05)。透射电镜结果显示,BEAS-2B细胞经2.0%CSE处理后出现线粒体萎缩变小,线粒体双层膜密度增高,线粒体脊减少甚至消失等典型铁死亡线粒体超微结构改变。细胞OD值Fer-1组>Nec-1组、Z-VAD-FMK组、CSE组;Fer-1组细胞Fe^(2+)、ROS水平低于CSE组,GSH水平高于CSE组;Fer-1组细胞FTH1、GPx4 mRNA及蛋白高于CSE组,Ptgs2 mRNA及蛋白低于CSE组;细胞死亡率Fer-1组低于CSE组(P均<0.05)。结论烟草烟雾暴露可诱导BEAS-2B细胞发生铁死亡,该作用可能通过介导BEAS-2B细胞铁超载和氧化还原紊乱来实现。

大学校园室内大气NO_(2)污染特征及学生暴露水平

采用被动法监测沈阳某高校校园学生寝室、教室、南门和北门门卫室、食堂室内大气NO_(2)两周平均质量浓度的季节变化特征,同时记录临近空气质量监测站室外NO_(2)小时平均质量浓度,评估学生NO_(2)暴露水平.结果表明:食堂的室内NO_(2)质量浓度最高(106.7~321.2μg/m^(3)),南门和北门门卫室次之(分别为30.5~148.3μg/m^(3)和39.3~138.9μg/m^(3)),学生寝室和教室最低(分别为22.1~40.9μg/m^(3)和22.6~42.2μg/m^(3));食堂和门卫室室内NO_(2)质量浓度具有明显的季节变化特征,各季节的NO_(2)质量浓度基本呈现冬季>秋季和春季>夏季的特征;燃气和香烟的燃烧分别是食堂和门卫室室内大气NO_(2)的重要来源,可引起较严重的室内NO_(2)污染;学生NO_(2)暴露水平为26.5~53.3μg/m^(3),表明学生基本不受NO_(2)污染影响.通过加强食堂室内外通风,缩短在食堂的停留时间等可降低学生的NO_(2)暴露水平.

Prevalence and Determinants of Secondhand Smoke Exposure Among Adolescent Girls-China,2019

Summary What is already known about this topic?The rate of secondhand smoke(SHS)exposure among female junior high students in 2013-2014 in China was 69.9%.What is added by this report?The rate of SHS among adolescent girls in 2019 in China was 62.8%,with 60.8%in junior high and 65.3%in senior high school,meanwhile,higher SHS exposure was correlated to higher grade levels,senior high school over junior high school,urban areas,those with more pocket money,those who’ve attempted smoking,exposure to tobacco advertisements,those with parents who smoke,those with close friends who smoke,use of e-cigarettes,and belief that SHS exposure is detrimental to health.What are the implications for public health practice?The rate of SHS exposure among adolescent girls in China still remains extraordinarily high.Targeted public health initiatives to curb SHS exposure among adolescent girls are urgently needed in China.

Nose-only cigarette smoke exposure plus airway lipopolysaccharide inhalation induced chronic obstructive pulmonary disease and associated pulmonary hypertension in mice

Objective To establish a mouse model of chronic obstructive pulmonary disease(COPD)and associated pulmonary hypertension(COPD-PH)induced by noseonly cigarette smoking exposure plus airway lipopolysaccharide(LPS)inhalation.Methods There were 24 male C57B6 mice divided into a control group and a